Plant senescence is a series of biochemical and physiological phenomena occurring in the last stage of the post-embryonic development of a plant, limiting the longevity of individual plants. The initiation of plant senescence is a turning point at which a drastic change occurs within cells, and the plants which are undergoing senescence decline in synthetic ability and have cellular structures and macro molecules degraded so as to lose cellular homeostasis, leading to cell death (Matile P. et al., Elservier, 413-440, 1992; Nooden L. D. et al., Academic press, 1988; Thiman K. V. et al., CRC press, 85-115, 1980; Thomas H. et al., Annu. Rev. Plant Physiol. 123:193-219, 1993). Plant senescence is not a simple passive degradation process of plant organs, but genetically programmed as a highly elaborated and active process that proceeds in cells, tissues, and organs.
In addition to biological importance, plant senescence is of industrial importance because it is relevant to the improvement of crop productivity and storability after harvest. Accordingly, genetic, molecular biological, physiological, and biochemical research has been actively conducted on plant senescence. However, most reports were obtained from research on plant hormones, and senescence regulation, such as the use of senescence regulating genes, has yet to be studied sufficiently.
Through reverse genetic methods, about 100 genes that increase in expression during leaf senescence have been found so far in mouse-ear cress, tomato, corn, rice, tobacco, and potato plants (Buchanan-Wallaston, J. Exp. Bot. 48: 181-199, 1997; Quirini et al., Trends Plant Sci. 5: 278-282, 2000). However, the functions of only a small number of the senescence-associated genes have been studied, with the properties of most remaining unknown. Recently, mutants that delay senescence have been isolated and studied in an attempt to find genes responsible for the regulation of leaf senescence (Woo H. R. et al., Plant Cell 13: 1779-1790, 2001; Woo H. R. et al., Plant J. (in press)). However, experimental difficulties have prevented senescence regulating genes from being isolated from senescence-promoting mutants.